We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Aged polylactic acid microplastics exacerbate lipid metabolism disorders and cardiac dysfunction via PPARγ activation in zebrafish: A comparative study with polymers and oligomers
Summary
Researchers compared the toxicity of polylactic acid microplastics at different degradation stages—polymers, oligomers, and aged polymers—in zebrafish larvae, finding that aged PLA most severely disrupted lipid metabolism and cardiac function through PPARγ activation.
Polylactic acid (PLA), a biodegradable plastic, is increasingly promoted as a sustainable alternative to conventional plastics. However, its degradation under non-composting conditions and associated toxicological impacts remain insufficiently understood. This study aimed to compare the toxicity of PLA microplastics (MPs) at different degradation stages, including PLA polymers, oligomers, and aged polymers, in zebrafish larvae. Zebrafish were exposed to environmentally relevant concentrations (0.1, 1, and 10 mg/L), and morphological, biochemical, and transcriptomic analyses were performed. PLA MPs disrupted lipid metabolism, decreased ATP levels, and elevated reactive oxygen species production, ultimately leading to cardiac malformations. Mechanistically, PLA MPs activated the peroxisome proliferator-activated receptor γ (PPARγ), upregulating genes related to lipid storage and cardiac development. Co-exposure with a PPARγ antagonist GW9662 partially alleviated these effects, confirming the role of PPARγ-mediated pathways in PLA MP-induced lipid disruption and cardiotoxicity. Notably, PLA polymers showing stronger cardiac dysfunction than PLA oligomers and ultraviolet (UV)-aged PLA polymers. These findings provided critical evidence that PLA MPs impair energy homeostasis and cardiac development in zebrafish, underscoring the urgent need for comprehensive ecological risk assessments of PLA-based materials under realistic environmental conditions.
Sign in to start a discussion.
More Papers Like This
Lipid metabolic dysregulation: A novel developmental toxicity pathway of aged nanoplastics via inhibition of lipophagy in zebrafish
Researchers showed that UV-aged polystyrene nanoplastics cause more severe developmental toxicity in zebrafish larvae than pristine particles by blocking lipophagy — the cellular process of breaking down stored fat via lysosomes — leading to abnormal lipid accumulation and disrupted early development.
Polylactic acid microplastics before and after aging induced neurotoxicity in zebrafish by disrupting the microbiota-gut-brain axis
Researchers exposed zebrafish to microplastics made from PLA, a common biodegradable plastic, and found that both new and aged PLA particles caused brain and nerve damage, including sluggish behavior, memory problems, and increased aggression. Aged PLA particles were even more toxic, and the damage appeared to work through disruption of the gut-brain connection, raising concerns about the safety of biodegradable plastics as they break down in water.
Multiple endpoints of polylactic acid biomicroplastic toxicity in adult zebrafish (Danio rerio)
Researchers exposed adult zebrafish to polylactic acid (PLA) bioplastic microparticles for 30 days and found accumulation in liver, brain, gills, and tissue, along with social behavior disruption, cholinergic changes, oxidative imbalance, and altered pigmentation — challenging the assumption that biodegradable bioplastics are environmentally benign.
Behavioral and biochemical consequences of Danio rerio larvae exposure to polylactic acid bioplastic.
Zebrafish larvae exposed to polylactic acid (PLA) bioplastic particles for five days showed behavioral changes including altered locomotion and biochemical disruptions — and the particles accumulated in the larvae. The results indicate that PLA bioplastics are not harmless to aquatic life and deserve the same ecological scrutiny as petroleum-based plastics.
Assessment on intestinal health from polylactic acid microplastics degradation on rare minnow (Gobiocypris rarus): Inflammation regulation by mitochondrial dysfunction
Researchers exposed rare minnow fish to photodegraded polylactic acid microplastics to assess intestinal health effects. The study found that these biodegradable plastic particles induced visible intestinal damage, triggered inflammation through mitochondrial dysfunction, and caused oxidative stress, suggesting that even biodegradable plastics may pose ecological risks after environmental degradation.